Currently, there are no biomarkers to predict the drug response, and the mechanisms of resistance are poorly characterised in HNSCC.40,43 In a recent time, course study to investigate the transcriptional and DNA methylation signatures driving acquired cetuximab resistance in HNSCC, we found that an essential driver of resistance to anti-EGFR-targeted therapies, FGFR1, is epigenetically regulated during chronic exposure to cetuximab and provide strong evidence that epigenetic alterations can drive acquired resistance.10 Here, FGFR1 is linked to head and neck squamous cell carcinoma.